K. M. Aird

This study shows GPX3 is necessary for ovarian cancer growth in vivo and promotes GDF15 expression, linking it to immune checkpoint inhibitor response.

This study shows that chemotherapy-induced senescence-associated secretome promotes metastasis in ovarian cancer by reprogramming metabolism and increasing cell detachment.

This study shows ATR enhances mTORC1 activity through cholesterol synthesis via LSS, independent of CHK1 and TSC, and this effect is amplified in p16-deficient cells.

This study identifies an alternative splice variant of Drp1 in ovarian cancer that promotes metastasis and chemoresistance by altering mitochondrial dynamics.

This study shows that tumor-associated macrophages (TAMs) enhance ovarian cancer stem-like cell (OvCSC) proliferation and survival, contributing to chemotherapy resistance and relapse.

This study identifies de novo purine metabolism as a vulnerability in cancers with low p16 expression, showing sensitivity to anti-folate drugs like methotrexate.

This study shows that thymidine rescues ATR kinase inhibitor-induced deoxyuridine contamination, cell death, and Type 1 interferon expression in CD8+ T cells.

This study shows that DOT1L regulates the senescence-associated secretory phenotype (SASP) through epigenetic control of IL1A expression in oncogene-induced senescence.

This study shows that reducing p16 expression lowers SASP factor and cytokine levels in senescent cells without affecting senescence markers.

This study shows that combining ATM inhibitors with fenofibrate improves treatment in high-grade serous ovarian cancer cells by inducing senescence.

This study shows that ATM inhibition promotes cancer cell survival by increasing macropinocytosis, which can be suppressed by BCAA supplementation.

This study identifies NFATC4 as a regulator of quiescence and chemotherapy resistance in ovarian cancer, showing its role in promoting a non-proliferative state and poor prognosis.

This study shows that p16 suppression increases nucleotide synthesis through mTORC1 activation, promoting tumorigenesis by bypassing senescence.

This study shows that SIRT3 activation is required for ovarian cancer cell survival and metastasis by regulating mitochondrial antioxidant defenses and metabolic changes during detachment.

This study identifies IDH1 as a therapeutic target in HGSC by showing its role in promoting metabolic adaptation and epigenetic repression, leading to senescence when inhibited.

This paper develops a method to simultaneously quantify and trace dNTP metabolites using isotope dilution and high-resolution mass spectrometry, showing improved accuracy and metabolic pathway insights.